Биология ва тиббиёт муаммолари 2026, №2 (168)
Subject of the article
OXIDATIVE STRESS AND MORPHOLOGICAL ALTERATIONS IN THE UTERUS DURING CHRONIC CARBON MONOXIDE EXPOSURE (278-284)
Authors
Ruzieva Gulrukh Maratovna
Institution
Bukhara State Medical Institute, Republic of Uzbekistan, Bukhara
Abstract
Carbon monoxide (CO) is one of the most prevalent toxic environmental pollutants formed during the incomplete combustion of carbon-containing materials. Owing to its high affinity for hemoglobin (more than 200 times greater than that of oxygen), CO forms carboxyhemoglobin (COHb), which significantly impairs the oxygen-carrying ca-pacity of blood and induces tissue hypoxia. Although the systemic effects of acute and chronic CO poisoning have been extensively investigated in the cardiovascular and central nervous systems, the impact of chronic low-dose CO exposure on the female reproductive system, particularly on the morphological and biochemical state of the uterus, remains insufficiently characterized. The aim of the present experimental study was to investigate the mor-phological and morphometric alterations in uterine tissues, as well as oxidative stress parameters, induced by chronic exposure to carbon monoxide in laboratory animals. The study was performed on 40 female white labora-tory rats divided into one control and three experimental groups exposed to 50, 100, and 200 ppm of CO over 30 days. Histological evaluation was performed using hematoxylin–eosin staining, while morphometric analysis in-cluded measurement of endometrial thickness, the number of uterine glands, and vascular density. Oxidative stress was assessed by quantitative determination of malondialdehyde (MDA) and superoxide dismutase (SOD) activity. The results revealed a statistically significant dose-dependent decrease in endometrial thickness from 420 ± 18 μm in the control group to 285 ± 15 μm at 200 ppm (p < 0.001), accompanied by a reduction in the number of uterine glands from 28 ± 2 to 14 ± 2 (p < 0.001). MDA levels increased by 168% relative to control, while SOD activity de-creased by 62%, indicating significant pro-oxidant–antioxidant imbalance. Conclusion: Chronic exposure to car-bon monoxide induces dose-dependent structural remodeling of uterine tissues and disturbs the redox homeostasis of the endometrium and myometrium. These changes may compromise reproductive function and represent a previ-ously underestimated environmental risk factor for women of reproductive age.
Key words
carbon monoxide, uterus, endometrium, oxidative stress, hypoxia, malondialdehyde, superoxide dismutase, repro-ductive toxicology, experimental morphology.
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